The effect of oleate, linoleate, and EPA/DHA supplementation of postmenopausal women on in vivo lipid peroxidation and LDL susceptibility to ex vivo oxidation Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/th83m2182

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  • While replacement of dietary saturated fat with unsaturated fat has been advocated to reduce cardiovascular disease risk, diets high in polyunsaturated fatty acids (PUFA) could increase low density lipoprotein (LDL) susceptibility to oxidation, potentially contributing to the pathology of atherosclerosis. To assess in vivo lipid peroxidation and susceptibility, of LDL surface and core lipids to ex vivo oxidation, in women consuming increased amounts of specific unsaturated fatty acids, 15 postmenopausal women took daily supplements of sunflower oil providing 12.3 g/day of oleate, safflower oil providing 10.5 g/day of linoleate, and fish oil providing 2.0 g/day of eicosapentaenoate (EPA) and 1.4 g/day of docosahexaenoate (DHA) during a crossover trial. Plasma F₂-isoprostanes (F₂-isoP), malondialdehyde (MDA), and thiobarbituric acid reacting substances (TEARS) were measured to assess lipid peroxidation in vivo. Ex vivo oxidation of LDL was monitored by measuring the formation of phosphatidylcholine hydroperoxides (PCOOH) and cholesteryl linoleate hydroperoxides (CE18:200H) during coppermediated oxidation. Plasma free F₂-isoP and MDA concentrations were lower after EPA/DHA supplementation than after oleate (P = 0.001, F₂-isoP and 0.02, MDA) and linoleate supplementation (P = 0.04 for both F₂-isoP and MDA). However, plasma TBARS concentrations were higher after EPA/DHA than after oleate (P = 0.001) and linoleate supplementation (P = 0.0004). During LDL oxidation, the lag phase for PCOOH formation was shorter in EPA/DHA- than oleate- (P = 0.0001) and linoleate-enriched LDL (P = 0.002), while the lag phase for CE18:200H was shorter in EPA/DHA- than oleate- (P = 0.01) but not linoleate-enriched LDL. The maximal rate of PCOOH formation was lower in EPA/ DHA- than linoleate- (P = 0.007) but not oleate-enriched LDL, while the maximal rate of CE18:200H formation was lower in EPA/DHA- than oleate- (P = 0.03) and linoleate-enriched LDL (P [less than or equal to] 0.0001). The maximal concentrations of PCOOH and CE18:200H were lower in EPA/DHA- than oleate- (P [less than or equal to] 0.05) and linoleate-enriched LDL (P [less than or equal to] 0.01). Oleate-enrichment generally decreased the oxidative susceptibility of LDL surface and core lipids, while EPA/DHA-enrichment did not increase LDL oxidative susceptibility compared to linoleate-enrichment. This study emphasizes the need for more than one relevant assay of in vivo lipid peroxidation.
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